A single acute exposure to carbon monoxide in 5-day-old rats produces brain pathology of which one symptom is hyperactive behavior from which the animals recover at maturity. An identical exposure of adults produces hyperactivity from which the animals do not recover. The studies proposed here will examine the neurochemical correlates of the development of hyperactivity in both neonates and adult animals. Special emphasis will be placed upon the neurochemistry of the recovery period in the developing animals and upon the residual neurochemical damage in the neonatally-exposed and adult-exposed animals. The neurochemical studies will be concentrated upon the proposed transmitter substances, norepinephrine, dopamine, 5-hydroxytryptamine, Gaba and glutamate. The two types of hyperactivity will be tested for similarity in responsiveness to amphetamine since amphetamine may produce "paradoxical" effects in hyperactivity. The data from these studies are also seen as beginnings to the following broad questions: 1) Is there a motor activity regulating system which involves a cortical-caudato-pallido-subthalamic-thalamo-cortical circuit? 2) What , if any, are the neurochemical bases for the hyperactivity which commonly results from brain damage and are common neurotransmitter systems involved in both the developing and adult animal? 3) What neurochemical processes are correlated with the ability of neonatally brain damaged animals to return toward normal with maturation?